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Mediators of Inflammation
Volume 2012, Article ID 879419, 8 pages
Research Article

Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver

1Ciências Médicas, Programa de Pós-Graduação em Medicina, Universidade Federal do Rio Grande do Sul (UFRGS), 90035-903 Porto Alegre, RS, Brazil
2Hospital de Clínicas de Porto Alegre (HCPA), Universidade Federal do Rio Grande do Sul, 90035-903 Porto Alegre, RS, Brazil
3Faculdade Cenecista de Bento Gonçalves, 95700-973 Bento Gonçalves, RS, Brazil
4Programa de Pós-Graduação em Ciências Pneumológicas, Universidade Federal do Rio Grande do Sul (UFRGS), 90035-903 Porto Alegre, RS, Brazil
5Universidade Luterana do Brasil, 92425-900 Canoas, RS, Brazil

Received 22 September 2012; Revised 15 October 2012; Accepted 28 October 2012

Academic Editor: Fábio Santos Lira

Copyright © 2012 Darlan Pase da Rosa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sleep apnea is a breathing disorder that results from momentary and cyclic collapse of the upper airway, leading to intermittent hypoxia (IH). IH can lead to the formation of free radicals that increase oxidative stress, and this mechanism may explain the association between central sleep apnea and nonalcoholic steatohepatitis. We assessed the level of inflammation in the lung and liver tissue from animals subjected to intermittent hypoxia and simulated sleep apnea. A total of 12 C57BL/6 mice were divided into two groups and then exposed to IH ( ) or a simulated IH (SIH) ( ) for 35 days. We observed an increase in oxidative damage and other changes to endogenous antioxidant enzymes in mice exposed to IH. Specifically, the expression of multiple transcription factors, including hypoxia inducible factor (HIF-1 ), nuclear factor kappa B (NF- B), and tumor necrosis factor (TNF- ), inducible NO synthase (iNOS), vascular endothelial growth factor (VEGF), and cleaved caspase 3 were shown to be increased in the IH group. Overall, we found that exposure to intermittent hypoxia for 35 days by simulating sleep apnea leads to oxidative stress, inflammation, and increased activity of caspase 3 in the liver and lung.